Tkp 45 302 70 2009
Spinal cord injury (SCI) induces an immune response during which microglia, the resident immunocompetent cells of the central nervous system, become activated and migrate to the site of damage. Depending on their state of activation, microglia secrete neurotoxic or neurotrophic factors that influence the surrounding environment and have a detrimental or restorative effect following SCI, including causing or protecting bystander damage to nearby undamaged tissue. Subsequent infiltration of macrophages contributes to the SCI outcome.
We show here that suppressing microglia/macrophage activation using the tripeptide macrophage/microglia inhibitory factor (MIF/TKP) reduced secondary injury around the lesion epicenter in the murine dorsal hemisection model of SCI; it decreased the hypertrophic change of astrocytes and caused an increase in the number of axons present within the lesion epicenter. Moreover, timely inhibition of microglial/macrophage activation prevented demyelination and axonal dieback by modulating oligodendrocyte survival and oligodendrocyte precursor maturation. Microglia/macrophages located within or proximal to the lesion produced neurotoxic factors, such as tumor necrosis factor alpha (TNF-α).
These results suggest that microglia/macrophages within the epicenter at early time points post injury are neurotoxic, contributing to demyelination and axonal degeneration and that MIF/TKP could be used in combination with other therapies to promote functional recovery. Introduction Spinal cord injury (SCI) is a devastating trauma marked by the loss of sensory, motor and autonomic functions due to the degeneration of axons and glia.
The initial insult to the central nervous system (CNS) causes necrosis of cells within the lesion epicenter, thereby inducing a cascade of biochemical and cellular events that lead to demyelination, degeneration of spared axons and inflammatory immune responses collectively referred to as secondary damage (; ). The necrosis triggers glial cell (e.g. Astrocytes, oligodendrocyte precursor cells, and microglia) activation and recruitment to the site of injury. Glial cell activation and the subsequent gliotic scar formation are thought to drive the ensuing secondary damage.
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May 14, 2012 - MIF/TKP also inhibits microglial function in the CNS. With 14d MIF/TKP resulted in activation of ~45% of microglia. A., Gregg, T. And Lopes, R. Cambridge: Cambridge University Press, pp. Journal of Volcanology and Geothermal Research, 175, 45–59. Bulletin of Volcanology, 70, 563–582. Aeromagnetic constraints on the subsurface structure of Stromboli volcano. Geophysics, 35, 293–302.
In this setting, microglia, the resident CNS immune cells, release proinflammatory cytokines, reactive oxygen species and proteases that create bystander damage (; ). Chemokines produced by microglia, such as CCL2, CCL3, CXCL2/3 and CXCL10 are upregulated in minutes following injury (), recruit and activate peripheral polymorphonuclear leukocytes and monocytes which have been demonstrated to promote neurotoxicity (;;; ). On the other hand, the phagocytic properties of microglia and macrophages ensure myelin and tissue debris removal following the initial insult, which is necessary for proper remyelination of axons and neurite outgrowth (). In subsequent phases of the immune reaction, peripheral inflammatory cells such as neutrophils, macrophages and T-lymphocytes enter the lesioned area and release a plethora of cytokines that mediate detrimental effects through the generation of free radicals which promote apoptosis (). While there are some reports that suppression of the initial local inflammatory response following SCI reduces secondary injury around the lesion epicenter and improves functional outcome, other studies have provided evidence that inflammation supports regeneration via growth factors and cytokines released by activated microglia and macrophages.